scholarly journals Comparative study between two 2D-Shear Waves Elastography techniques for the non-invasive assessment of liver fibrosis in patients with chronic hepatitis C virus (HCV) infection

2021 ◽  
Author(s):  
Victor Bâldea ◽  
Felix Bende ◽  
Alina Popescu ◽  
Roxana Șirli ◽  
Ioan Sporea

Aims: We aimed to compare the diagnostic performance of two 2D-Shear Wave Elastography (2D-SWE) techniques for the non-invasive assessment of liver fibrosis in patients with chronic hepatitis C virus (HCV) infection using Transient Elas-tography (TE) as reference. Material and methods: We enrolled 208 consecutive patients with chronic HCV infection, in which liver stiffness (LS) was evaluated in the same session using two 2D-SWE techniques: 2D-SWE.GE and 2D-SWE.SSI using TE as the method of reference. LS measurements were considered failures when no value was obtained after 10 attempts. Results: Valid LSMs were obtained in 95.6% (199/208) of cases by 2D-SWE.GE, 92.7% (193/208) of cases by 2D-SWE.SSI, and in 94.7% (197/208) of cases by TE (p>0.05). The mean LS values by 2D-SWE.GE were significantly lower than those obtained by 2D-SWE.SSI: 10.3±3.8 kPa vs. 15±10.4 kPa (p<0.0001). 2D-SWE.GE LSMs correlated better with TE than 2D-SWE.SSI (r=0.75, p<0.0001 vs. r=0.57, p<0.0001, z test p=0.0012). Linear regression analysis showed a moderate correlation between LSMs obtained by 2D-SWE.GE and 2D-SWE.SSI (r=0.63, R2=0.4, P<0.0001). Pairwise comparison of receiver operating characteristics curves (ROC) found no significant differences between 2D-SWE.GE and 2D-SWE.SSI in identifying F≥2 fibrosis (0.97 vs. 0.96, P = 0.5650), F≥3 (0.97 vs. 0.95, P = 0.2935), or F=4 (0.97 vs. 0.96, p = 0.6914). Conclusions: Both 2D-SWE techniques had good feasibility for the noninvasive assessment of liver fibrosis. LS values obtained by 2D-SWE.GE were significantly lower than those obtained by 2D-SWE.SSI. No significant differences were found between both methods in staging liver fibrosis in patients with chronic HCV.

2014 ◽  
Vol 8s3 ◽  
pp. CMC.S17069 ◽  
Author(s):  
Nobukazu Ishizaka ◽  
Yuko Ishizaka ◽  
Minoru Yamkado

Chronic infection and associated inflammation may play a role in various unfavorable pathologic conditions, including atherosclerosis. Chronic hepatitis C virus (HCV) infection is thought to be associated with a higher prevalence of atherosclerotic vascular changes in the coronary artery, cerebrovascular artery, and carotid artery; however, little is known about the precise mechanisms by which HCV enhances atherogenic processes. Furthermore, some studies have found no association, or even an inverse association, between HCV infection and atherosclerotic vascular changes or cardiovascular events. Differences in data regarding the mode of association may be because of variations in sample size, target population, and study design. Nevertheless, physicians should be aware of cardiovascular disorders as a possible comorbidity – owing to their considerable consequences – among patients with chronic HCV infection.


2006 ◽  
Vol 59 (11-12) ◽  
pp. 560-566
Author(s):  
Ivanko Bojic ◽  
Ljubisa Dokic ◽  
Svetlana Minic

Introduction. The incidence of chronic hepatitis C virus (HCV) infection is rather high. Its most frequent consequences are chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Treatment of chronic HCV infection. In treatment of chronic HCV infection, interferons have antiviral, anriproliferative, and immunoregulatory action. Within the cell, they induce protein synthesis, inhibiting viral replication. The most important among them are RNA dependent protein kinase, and eukaryotic initiation factor. However, viral proteins prevent their phosphorylation and activation. In order to overcome this problem, treatment is prolonged, higher doses of IFN are used, as well as induction therapy. The optimal period for viral response is 52 weeks, while induction therapy has shown controversial results. .


2008 ◽  
Vol 82 (21) ◽  
pp. 10896-10905 ◽  
Author(s):  
Jin-Won Youn ◽  
Yu-Wen Hu ◽  
Nancy Tricoche ◽  
Wolfram Pfahler ◽  
Mohamed Tarek Shata ◽  
...  

ABSTRACT Given the failures of nonreplicating vaccines against chronic hepatitis C virus (HCV) infection, we hypothesized that a replicating viral vector may provide protective immunity. Four chimpanzees were immunized transdermally twice with recombinant vaccinia viruses (rVV) expressing HCV genes. After challenge with 24 50% chimpanzee infective doses of homologous HCV, the two control animals that had received only the parental VV developed chronic HCV infection. All four immunized animals resolved HCV infection. The difference in the rate of chronicity between the immunized and the control animals was close to statistical significance (P = 0.067). Immunized animals developed vigorous gamma interferon enzyme-linked immunospot responses and moderate proliferative responses. To investigate cross-genotype protection, the immunized recovered chimpanzees were challenged with a pool of six major HCV genotypes. During the acute phase after the multigenotype challenge, all animals had high-titer viremia in which genotype 4 dominated (87%), followed by genotype 5 (13%). However, after fluctuating low-level viremia, the viremia finally turned negative or persisted at very low levels. This study suggests the potential efficacy of replicating recombinant vaccinia virus-based immunization against chronic HCV infection.


Author(s):  
OV Churbakova ◽  
VG Akimkin ◽  
VV Pavlov ◽  
DV Pechkurov

Introduction: The ongoing adverse situation with the prevalence of chronic hepatitis C virus (HCV) infection makes it especially relevant to assess the epidemiological situation of this infection in the country as a whole and the Samara Region. Our objective was to determine characteristics of the epidemic process of chronic HCV infection in the territory of the Russian Federation and the Samara Region in 1997–2018. Results and discussion: We observed a dynamic 5.88-fold increase in the Russian rates of chronic HCV infection in 1997–2014 from 6.7 0/0000 to 39.4 0/0000 (p < 0.01) followed by a decrease by 16.5 % in 2015–2018 (from 39.2 0/0000 to 32.7 0/0000). In the Samara Region, we traced a periodic wave-like increase alternating with small drops in the prevalence rates during the whole observation period. In 1997–2016, the rates of chronic HCV infection rose from 5.2 0/0000 to 58.0 0/0000 (by 11.2 times; p < 0.01) and declined slightly from 58.0 0/0000 to 56.2 0/0000 in 2016–2018. The maximum rates of chronic HCV infection in the child population of the Samara Region were registered in 2002 and 2012 (7.1 0/0000 and 7.2 0/0000, respectively) with the minimum of 1.9 0/0000 noted in 2017. The analysis of the epidemiological situation of chronic hepatitis is important for subsequent trend forecasting and developing appropriate preventive measures.


2011 ◽  
Vol 152 (22) ◽  
pp. 876-881
Author(s):  
Alajos Pár

The review discusses the genetic polymorphisms involved in the pathogenesis of hepatitis C virus (HCV) infection, that may determine the outcome of disease. In this field earlier both certain major histocompatibility complex (MHC) alleles and some cytokine gene variants have also been studied. Recently, the genome-wide association study (GWAS) and targeted single nucleotide polymorphism (SNP) analysis have revealed that a variant in the promoter region of interleukin-28B (IL-28B) gene is strongly linked to viral clearance and it may be the strongest pretreatment predictor of treatment response in chronic hepatitis C. Last year it was shown that two genetic variants leading to inosine triphosphatase deficiency protect against haemolytic anemia in patients receiving ribavirin during antiviral treatment for chronic HCV infection. Orv. Hetil., 2011, 152, 876–881.


2019 ◽  
Vol 2 (1) ◽  
pp. 23-30
Author(s):  
Mark Collister ◽  
Julia Rempel ◽  
Jiaqi Yang ◽  
Kelly Kaita ◽  
Zach Raizman ◽  
...  

Background: Interleukin 32 (IL-32) is a recently described pro-inflammatory cytokine implicated in chronic hepatitis C virus (HCV)-related inflammation and fibrosis. IL-32α is the most abundant IL-32 isoform. Methods: Circulating IL-32α levels were documented in patients with chronic HCV infections ( n = 31) and compared with individuals who spontaneously resolved HCV infection ( n = 14) and HCV-naive controls ( n = 20). In addition, peripheral blood mononuclear cells (PBMC) from the chronic HCV ( n = 12) and HCV-naive ( n = 9) cohorts were investigated for responses to HCV core and non-structural (NS)3 protein induced IL-32α production. Finally, correlations between IL-32α levels, hepatic fibrosis and subsequent responses to interferon-based therapy were documented in patients with chronic HCV. Results: Circulating IL-32α levels in patients with chronic HCV were similar to those of spontaneously resolved and HCV-naive controls. HCV protein induced IL-32α responses were similar in chronic HCV patients and HCV-naive controls. In patients with chronic HCV, serum IL-32α levels correlated with worsening METAVIR fibrosis (F) scores from F0 to F3 ( r = 0.596, P < 0.001) as did NS3 induced IL-32α responses ( r = 0.837, P < 0.05). However, these correlations were not sustained with the inclusion of IL-32α levels at F4 scores, suggesting events at F4 interfere with IL-32α synthesis or release. In chronic HCV patients who underwent treatment ( n = 28), baseline in vivo and in vitro induced IL-32α concentrations were not predictive of therapeutic outcomes. Conclusions: IL-32α activity is associated with worsening fibrosis scores in non-cirrhotic, chronic HCV patients.


2018 ◽  
Vol 67 (3) ◽  
pp. 681-685 ◽  
Author(s):  
Ali Sobhy ◽  
Mohammed Fakhry M. ◽  
Haitham A Azeem ◽  
Ahmed M Ashmawy ◽  
Hamed Omar Khalifa

Several studies were performed to evaluate the degree of liver fibrosis by non-invasive markers. We aimed to assess the diagnostic value of both biglycan (BGN) and osteopontin (OPN) as non-invasive markers of hepatic fibrosis in patients with chronic hepatitis B (CHB) and chronic hepatitis C (CHC). This study was performed on 100 patients with CHB virus, 100 patients with CHC virus and 100 normal controls. All participants were subjected to the following laboratory tests: hemoglobin, platelet, alanine aminotransferase, aspartate aminotransferase, albumin, international normalized ratio, HBs Ag, hepatitis C virus (HCV) antibody, hepatitis B virus DNA, HCV RNA, liver biopsy, BGN and OPN. We found that BGN level was significantly increased in the CHB group compared with the controls (p<0.001), but the level was not different between the CHC group and the controls (p<0.96). OPN was increased in both the CHB and CHC groups compared with the controls (p<0.001). Positive correlation was found between fibrosis stages and BGN level of the CHB group (r=0.64; p<0.001) and between fibrosis stages and OPN level of the CHB (r=0.63; p<0.001) and CHC (r=0.59; p<0.03) groups. The area under the curve (AUC), sensitivity and specificity of BGN were 1.0, 100% and 100% in predicting fibrosis in patients with CHB, and 0.50, 26% and 78% in predicting fibrosis in patients with CHC. OPN had an AUC of 0.997, sensitivity of 96% and specificity of 100% in predicting fibrosis in patients with CHB, and 0.974, 96.5% and 100% in predicting fibrosis in patients with CHC. In conclusion, BGN and OPN could be considered non-invasive markers for liver fibrosis assessment.


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